Strategies for antiviral drug design have typically focused on identifying compounds that attack the virus itself. As such, the most common antiviral targets have been viral proteins—the structural components of the virion, as well as viral genome-encoded enzymes which are necessary for propagation of the virus. Thus, antiviral compounds have been designed and developed to interfere with viral proteins involved in attachment of the virus to the host cell membrane and entry into the cell, replication, transcription and translation of the viral genes, propagation of the virion inside the cell, and/or release of progeny virions from the cell.
Nevertheless, the approach of targeting viral proteins has several limitations: 1) the limited number of viral targets; 2) viral targets tend to be highly specific to a particular virus or even strain of virus; and 3) the ability of viruses to rapidly alter their genetic composition to develop resistance to antiviral drugs.
Another approach in antiviral drug development is to design drugs to strengthen the host's immune system to fight the viral infection, rather than to fight the viral infection itself. Using this strategy, drugs are designed to boost the host's immune system to allow the host to better fight off infection by the virus.
On the other hand, cellular targets have traditionally been considered less desirable candidates for antiviral therapy. Relatively few antiviral drugs have been directed at host enzymes for several reasons, the most prominent being the high risk of toxicity to the host itself. Although host cell factors play a key role in facilitating viral growth and propagation, strategies for attacking such host factors remain elusive.
A major challenge to antiviral drug development is finding new strategies for combating viral infection.